Visual agnosia is a neuropsychological syndrome characterized by a failure of object identification. Apperceptive agnosia, an object identification deficit caused by damage to early perceptual processes, has been explained by appealing to both damaged early sensory processes and to damaged preattentive grouping processes. Which of these two explanations best accounts for the behavior of these patients? We present results from two experiments designed to distinguish rival theoretical accounts of apperceptive agnosia. In our studies, we attempted to simulate apperceptive agnosia in neurologically intact subjects. Sensory-deficit accounts of the syndrome predict that degrading visual processing would make normal subjects perform like patients; grouping-deficit accounts predict that removing perceptual organization cues from visual displays would make normal subjects perform like patients. We were able to simulate the behavior of an apperceptive agnosic patient by removing perceptual organization cues, consistent with a grouping-deficit account of this syndrome. The implications for understanding both apperceptive agnosia and normal visual functioning are discussed.

The posterior visual spatial attention system involves a number of separable computations that allow orienting to visual locations. We have studied one of these computations, inhibition of return, in 3-, 4-, 6-, 12-, and 18--month-old infants and adults. Our results indicate that this computation develops rapidly between 3 and 6 months, in conjunction with the ability to program eye movements to specific locations. These findings demonstrate that an attention computation involving the mid-brain eye movement system develops after the third month of life. We suggest how this development might influence the infant's ability to represent and expect visual objects.